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Vesiculo bullous I


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Oral Pathology I
Third Year

Published in: Health & Medicine
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Vesiculo bullous I

  1. 1. Vesiculo-Bullous Diseases Aiman A. Ali DDS, PhD.
  2. 2. Vesiculo-Bullous Diseases    Viral Associated with immunologic defects Hereditary Aiman A. Ali DDS, PhD.
  3. 3. Viral infections of significance to clinical dentistry Aiman A. Ali DDS, PhD.
  4. 4. Viral infections of significance to clinical dentistry  Herpes Simplex Virus (HSV) infection  Varicella-Zoster infections  Hand, Foot, and Mouth Disease  Herpangina  Measles (Rubeola) Aiman A. Ali DDS, PhD.
  5. 5. Herpes Simplex Virus (HSV) infection Pathogenesis  DNA virus.  Two types HSV1 & HSV2  Transmitted by physical contact with an infected person  Travel through the trigeminal nerve to the t. ganglion  Become latent in the neural tissue  With reactivation it travels to the epithelial surface  Reactivation by exposure to sunlight [fever blister] or exposure to cold [cold blister] or other factors. Aiman A. Ali DDS, PhD.
  6. 6. Precipitating Factors Stress Nutrition Trauma Hormonal Diet Immunologic
  7. 7. Herpes Simplex Virus (HSV) infection Clinical features (Primary)  Primary herpetic gigivostomatitis  Usually affects children  Vesicular eruption may appear on the skin vermilion  In the oral cavity, lesions may appear on any part of the oral mucosa  Viremia symptoms: fever, arthralgia, malaise, headache and cervical lymphadenopathy  After 7 to 10 days the lesions heal without scar Aiman A. Ali DDS, PhD.
  8. 8. Herpes Simplex Virus (HSV) infection Clinical features (Secondary) • Usually on the lip and rarely on gingiva or palate • Prodromal symptoms • Within hours multiple fragile vesicles appear • Lesions ulcerate and coalesce • Lesions heal without scaring in 1 to 2 weeks • Rarely become secondarily infected • Recurrence vary from 1 per year to 1 per month Aiman A. Ali DDS, PhD.
  9. 9. Herpes Simplex Virus (HSV) infection Clinical features (Whitlow)      Typically occur in dental practitioners who don’t use gloves and had physical contact with infected individuals Either primary or secondary HSVI involving the fingers Recurrent lesions if occurred, would be expected on fingers Pain, redness, vesicles that break to become ulcers Duration vary from 4 to 6 weeks Aiman A. Ali DDS, PhD.
  10. 10. Herpes Simplex Virus (HSV) infection Histopathology  Vesicles are intraepithelial  Some virus-infected epithelial cells are seen  After several days these features disappear Aiman A. Ali DDS, PhD.
  11. 11. Herpes Simplex Virus (HSV) infection Differential Diagnosis  Primary HSV infection  Streptococcal pharyngitis  Erythema multiform  ANUG  Secondary HSV infection  Recurrent aphthous stomatitis Aiman A. Ali DDS, PhD.  Virus culture, monoclonal antibodies or DNA hybridization
  12. 12. RIH RAS Appearance of primary lesion vesicle ulcer Appearance of mature lesion shallow, punctate ulcers ulcer (with erythematous halo) Common location attached gingiva, hard palate,vermillion border buccal mucosa, floor of mouth, oropharynx, vestibule, tongue Number few to several one to few Lesion duration 1-3 weeks 1-2 weeks Etiology Viral Unclear; immunologically mediated Prevalence (by adulthood) 70-80% (HSV-1) Possibly up to 66%
  13. 13. Herpes Simplex Virus (HSV) infection Treatment  Time is very important  Acyclovir • Oint 5% 5t. daily when symptoms first appear • Tab 200 to 400 mg 5t daily is effective  Vidarabine or Idoxuridine are effective on ocular HS but not LHS.  Primary HSV infection is best managed with supportive therapy [fluid, rest, oral lavage and antipyretics] Aiman A. Ali DDS, PhD.
  14. 14. Varicella-Zoster Infection Etiology & Pathogenesis  VZV is one of the herpes virus  Cause primary infection (varicella or chickenpox) and secondary disease (herpes zoster or shingles)  After primary infection, virus remain latent in a sensory ganglia  Reactivation of latent VZV usually follows immunosuppressive status, drug administration, irritation or local trauma Aiman A. Ali DDS, PhD.
  15. 15. Varicella-Zoster Infection Clinical features (Varicella)  Common  Fever, among children chills, malaise and headache  Rash involves the trunk, head & neck including oral mucosa  It develops into vesicles ulcerations  Lesions pustular heal after several weeks  Secondary infection is common Aiman A. Ali DDS, PhD.
  16. 16. Varicella-Zoster Infection Clinical features (Herpes Zoster) • Involvement of 5th nerve result in unilateral oral, facial, and ocular lesions • Prodromal symptoms of pain or paresthesia maculo-papular rash vesiculo-bullae Ulcerations heal after several weeks • Complications include • secondary infection • Post-herpetic neuralgia • Motor paralysis • Ocular inflammation Aiman A. Ali DDS, PhD.
  17. 17. Aiman A. Ali DDS, PhD.
  18. 18. Hunt’s Syndrome A special type of herpes zoster infection with involvement of the external ear and oral mucosa (facial and auditory nerves)
  19. 19. Varicella-Zoster Infection Histopathology  The same as those seen in HSV  Virus infected epithelial cells  Homogenous  In nuclei uncomplicated cases, epithelium regenerates with little or no scar Aiman A. Ali DDS, PhD.
  20. 20. Varicella-Zoster Infection Differential diagnosis  HSV infection: • Clinical features • Virus antigen typing using immunologic tests Aiman A. Ali DDS, PhD.
  21. 21. Varicella-Zoster Infection Treatment  Varicella: • Supportive therapy • In immunocompromised patients more substantial measures are indicated  Herpes zoster: • The same for HSV but in high dose • Acyclovir 800 mg x 5 x 7 to 10 days • Analgesics  Corticosteroids Aiman A. Ali DDS, PhD. are contraindicated
  22. 22. Hand foot & mouth disease Etiology & Pathogenesis  Coxsackie virus • CV type A • CV type B  A16, and occasionally A5, A9, A10, B2 and B5 cause HFM disease  HFM is a highly contagious infection  Virus transmission: through airborne spread or oral-fecal contamination Aiman A. Ali DDS, PhD.
  23. 23. Hand foot & mouth disease Clinical Features • Affect children under the age 5 years (epidemic) • Resolve spontaneously after 1 to 2 weeks • Signs and symptoms of viremia (low grade) • Oral lesions: multiple vesicles Ulcers covered by yellow membrane surround by erythema • Occur anywhere of the oral cavity • Hand and feet lesions are maculopapular with or shortly after the oral lesions vesicles ulcers Aiman A. Ali DDS, PhD.
  24. 24. Hand foot & mouth disease Histopathology  Vesicles are intraepithelial  The vesicle cavity filled with proteinaceous debris and inflammatory cells Aiman A. Ali DDS, PhD.
  25. 25. Hand foot & mouth disease Differential Diagnosis  Primary HSV infection and varicella: • Milder symptoms • Cutaneous distribution • Virus culture or detection of antibodies  Recurrent Aphthous Aiman A. Ali DDS, PhD.
  26. 26. Hand foot & mouth disease Treatment  Symptomatic Aiman A. Ali DDS, PhD. therapy
  27. 27. Herpangina Etiology & Pathogenesis  Coxsackie type A (A1-6, A8, A10, A22, B3 and possibly others)  Transmission through contaminated saliva Aiman A. Ali DDS, PhD.
  28. 28. Herpangina Clinical Features  Common in summer and in children  Pain, malaise, fever, dysphasia and sore throat  Oral vesicular eruption on the soft palate, faucial pillars and tonsils  Pharyngitis  Lesions last less than 1 week Aiman A. Ali DDS, PhD.
  29. 29. Herpangina Differential Diagnosis  HSV infection, HFM and varicella • Clinically • Short duration  Streptococcal Pharyngitis • Vesicular eruption • Summer presentation • Mild symptoms  Aphthous stomatitis • Systemic symptoms Aiman A. Ali DDS, PhD.
  30. 30. Herpangina Treatment  Treatment required Aiman A. Ali DDS, PhD. is usually not
  31. 31. Measles (Rubeola) Etiology & Pathogenesis  Highly contagious  Measles virus (DNA paramyxovirus) Aiman A. Ali DDS, PhD.
  32. 32. Measles (Rubeola) Clinical Features  Commonly affect children in winter and spring  incubation period of 7 to 10 days  Fever, malaise, conjunctivitis and cough  After 2 days small macules with white necrotic center (Koplik’s spots) appear in the buccal mucosa  After 2 days skin rash appear initially on the head and neck followed by the trunk and then the extremities Aiman A. Ali DDS, PhD.
  33. 33. Measles (Rubeola) Histopathology  Warthin-Frankeldey giant cells are seen in lymphoid tissue  Infected epithelial cells which become necrotic Aiman A. Ali DDS, PhD.
  34. 34. Measles (Rubeola) Diagnosis  Usually • • • • made on: Clinical signs and symptoms Prodromal symptoms Koplik’s spots If necessary, serologic test for antibodies to measles virus Aiman A. Ali DDS, PhD.
  35. 35. Measles (Rubeola) Differential Diagnosis M. Rubeola Rubella (German M.) • Paramyxovirus Family • Togavirus Family • Contagious • Contagious • (sever) Fever respiratory symptoms and rash • (mild) Fever, respiratory symptoms and rash • Koplik's spots • no Koplik's spots • Does not cause developmental abnormalities in the fetus • Cause developmental abnormalities in the fetus Aiman A. Ali DDS, PhD.
  36. 36. Measles (Rubeola) Treatment  Supportive treatment: • • • • Bed rest Fluids Adequate diet Analgesics Aiman A. Ali DDS, PhD.
  37. 37. ‫حادي العيس‬